Haemodynamic effects of physiological concentrations of circulating noradrenaline in man

Chang, P. C.; Kriek, E; Krogt, J. A. Van Der; Blauw, G. J.; Brummelen, P. Van

doi:10.1042/cs0750469

Cited by 12 publications

(13 citation statements)

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“…Dose-related blood flow responses to noradrenaline in skeletal muscle have been registered using forearm plethysmography. Low doses of noradrenaline increased the local blood flow, while the muscle was indifferent to high doses of noradrenaline [30]. In a recent study, the nutritive blood flow remained unaltered in adipose tissue and in skeletal muscle when sympathetic nerve activity was induced via lower body negative pressure [11].…”

Section: Discussionmentioning

confidence: 99%

Major differences in noradrenaline action on lipolysis and blood flow rates in skeletal muscle and adipose tissue in vivo

et al. 2005

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Aims/hypothesis: The regulation of skeletal muscle lipolysis is not fully understood. In the present study, the effects of systemic and local noradrenaline administration on lipolysis and blood flow rates in skeletal muscle and adipose tissue were studied in vivo. Methods: First, circulating noradrenaline levels were raised tenfold by a continuous i.v. infusion (n=12). Glycerol levels (an index of lipolysis) were measured in m. gastrocnemius and in abdominal adipose tissue using microdialysis. -10 −6 mol/l) (n=10). Local blood flow was monitored with the ethanol perfusion technique. Results: With regard to systemic noradrenergic stimulation, no change in fractional release of glycerol (difference between tissue and arterial glycerol) was seen in skeletal muscle. In adipose tissue it transiently increased twofold (p<0.0001), and the rate of appearance of glycerol in plasma showed the same kinetic pattern. Blood flow was reduced by 40% in skeletal muscle (p<0.005) and increased by 50% in adipose tissue (p<0.05). After noradrenaline stimulation in situ, a discrete elevation of skeletal muscle glycerol was registered only at the highest concentration of noradrenaline (10 −6 mol/l) (p<0.05). Adipose tissue glycerol doubled already at the lowest concentration (10 −8 mol/l) (p<0.05). In skeletal muscle a decrease in blood flow was seen at the highest noradrenaline concentrations (p<0.05). Conclusions/interpretation: Lipolysis and blood flow rates are regulated differently in adipose tissue and skeletal muscle. Adipose tissue displays a high, but transient (tachyphylaxia) sensitivity to noradrenaline, leading to stimulation of both lipolysis and blood flow rates. In skeletal muscle, physiological concentrations of noradrenaline decrease blood flow but have no stimulatory effect on lipolysis rates.

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Section: Discussionmentioning

confidence: 99%

Major differences in noradrenaline action on lipolysis and blood flow rates in skeletal muscle and adipose tissue in vivo

et al. 2005

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“…infusion (Chang et al 1988;Ensinger et al 1992;Goldenberg et al 1948;. Obviously, this represents an unphysiological approach: as a neurotransmitter noradrenaline is released from the sympathetic nerve terminal into the synaptic cleft and only a minor proportion of neuronally released noradrenaline will eventually "spill over" into the circulating blood (Goldstein et al 1986).…”

Section: Methodological Considerationsmentioning

confidence: 99%

Influence of adrenoceptor and muscarinic receptor blockade on the cardiovascular effects of exogenous noradrenaline and of endogenous noradrenaline released by infused tyramine

Schäfers¹,

Poller

Pönicke

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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This study aimed firstly to compare the in vivo cardiovascular effects of exogenously administered and of endogenously released noradrenaline; secondly to characterize the adrenoceptors mediating these responses; thirdly to assess the influence of parasympathetic tone on the cardiovascular effects of noradrenaline. In two randomised placebo-controlled studies, healthy, young, male volunteers received intravenous (i.v.) infusions of noradrenaline at six incremental doses of 10-160 ng/kg/min and-in order to release endogenous noradrenaline-tyramine at four incremental doses of 5-20 micrograms/kg/min. Noradrenaline and tyramine were administered in the absence and presence of alpha 1-adrenoceptor blockade with doxazosin (2 mg p.o.), alpha 2-adrenoceptor blockade with yohimbine (15 mg p.o.), selective beta 1-adrenoceptor blockade with bisoprolol (15 mg p.o.) and muscarinic receptor blockade with atropine (1.5 micrograms/kg i.v. loading dose followed by 0.15 microgram/kg/min by i.v. infusion). Vasoconstrictor effects were assessed by measurement of diastolic blood pressure (Pdiast) and myocardial effects by measurement of systolic time intervals, namely the duration of electromechanical systole corrected for heart rate (QS2c). I.v. noradrenaline increased Pdiast (delta max 17 mmHg) and this was nearly completely suppressed by doxazosin but only slightly blunted by yohimbine. Noradrenaline also slightly shortened QS2c (delta max -22 ms), and this was potentiated by both doxazosin and yohimbine and completely blocked by biosprolol. I.v. tyramine reduced Pdiast (delta max -7 mmHg), which was not affected by alpha 1-adrenoceptor blockade, and profoundly shortened QS2c (delta max -104 ms) which was significantly correlated with a marked increase in systolic blood pressure (Psyst) (delta max 57 mmHg). The shortening of QS2c and the rise in Psyst were not influenced by alpha-adrenoceptor blockade but were antagonized by bisoprolol. Atropine potentiated the blood pressure rise and the shortening of QS2c induced by i.v. noradrenaline and converted the fall in Pdiast induced by i.v. tyramine into an increase. Thus the cardiovascular effects of exogenous noradrenaline are mainly characterized by alpha 1-adrenoceptor-mediated vasoconstriction and the actions of endogenous noradrenaline (released by i.v. tyramine) by beta 1-adrenoceptor-mediated positive inotropic effects. The rise in Psyst with i.v. tyramine most likely reflects positive inotropism and not a vascular "pressor' response.

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“…The gradient reflects the neuronal and extraneuronal uptake of the catecholamines in the tissues during their IV administration. The baseline plasma concentrations of noradrenaline and adrenaline and the variance were in the range found in other studies [1,4,[8][9][10][11][12][13][14][15]. The study design was not optimised to obtain minimal variation.…”

Section: Discussionmentioning

confidence: 81%

“…The fractional extraction of noradrenaline, as shown by the slope of the arterio-venous concentration relationship, was 24 %, although other investigators have reported higher fractional extraction rates [2,4,8,16]. The forearm fractional extraction of noradrenaline was found to be dependent on the plasma noradrenaline concentration [8] and on forearm blood flow [4,17].…”

Section: Discussionmentioning

confidence: 93%

“…The forearm fractional extraction of noradrenaline was found to be dependent on the plasma noradrenaline concentration [8] and on forearm blood flow [4,17]. In all those studies, however, the fractional extraction was only investigated at a baseline plasma noradrenaline concentration using tracer techniques except by Chang et al [8], who employed infusion rates up to 0.054 gg. kg-~.…”

Section: Discussionmentioning

confidence: 97%

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Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers

Ensinger

Weichel

Lindner

et al. 1992

Eur J Clin Pharmacol

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Noradrenaline and adrenaline were infused IV at 5 different rates (0.01-0.2 micrograms.kg.min-1) for 30 min to volunteers. The plasma catecholamine concentrations were determined by HPLC and electro-chemical detection. At the highest infusion rate, the arterial and venous plasma concentrations of noradrenaline increased from 1.18 to 44.1 nmol.l-1 and from 1.14 to 31.9 nmol.l-1, respectively, and of adrenaline from 0.29 to 23.9 nmol.l-1 and from 0.28 to 19.3 nmol.l-1, respectively. The peripheral venous plasma concentration of noradrenaline averaged 76% of the arterial concentration, and of adrenaline it was 73%. There was a linear relationship between the peripheral venous and arterial plasma noradrenaline and adrenaline concentrations at therapeutic doses.

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Haemodynamic effects of physiological concentrations of circulating noradrenaline in man

Cited by 12 publications

References 0 publications

Major differences in noradrenaline action on lipolysis and blood flow rates in skeletal muscle and adipose tissue in vivo

Major differences in noradrenaline action on lipolysis and blood flow rates in skeletal muscle and adipose tissue in vivo

Influence of adrenoceptor and muscarinic receptor blockade on the cardiovascular effects of exogenous noradrenaline and of endogenous noradrenaline released by infused tyramine

Relationship between arterial and peripheral venous catecholamine plasma catecholamine concentrations during infusion of noradrenaline and adrenaline in healthy volunteers

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